Abstract

Background: Prostate cancer (PCa) is the second most common worldwide neoplasm in men [1]. Proliferative inflammatory atrophy (PIA) is proposed as a “risk factor lesion” as it has an important inflammatory component and the associated oxidative stress has been suggested to have a role in prostatic carcinogenesis [2,3]

Objectives: To determine correlations between pathological findings of inflammation and proliferative inflammatory atrophy (PIA), in prostate biopsy specimens and to compare their prevalence in biopsies with and without prostate adenocarcinoma.

Methods: A prospective study was conducted between December 2010 and June 2012 in the Hospital Universitario del Caribe, Cartagena, Colombia. Patients referred for transrectal ultrasound-guided prostate needle biopsy for suspected PCa were invited to participle and signed an informed consent. Initial prostate biopsies were examined for the presence of PCa, chronic inflammation and atrophy. The inflammation was scored for grade, localization and extension using the classification system of the CPCRN and IPCN consensus [4]. Atrophy was classified according to “Working Group Classification of Focal Prostate Atrophy Lesions” [5], and grade of atrophy was graduated using categories described by Postma [6]. For statistical analysis we compared parameters between groups with and without PCa. This study was approved for the Ethical Review Board of the participating institutions.

Results: 97 patients were included, between the ages of 47 and 87 years (mean age: 68.32, SD: 8.9). Adenocarcinoma was identified in 50 of the 97 (51.5%) biopsies examined. There was a significant age difference between the PCa and benign groups (p=0.0031) and PSA levels were significantly higher in patients with cancer. Inflammation was detected in 95.87% of biopsies. Inflammation grade was significantly different between PCa and benign samples (p=0.038) but extension and localization of inflammation was not different between the groups. PIA was observed in 61 cases (62.8%) of which 23 had PCa. Atrophy grade and type were not different between groups and simple atrophy was the most frequently observed type. Morphological transition PIA-HGPIN was significantly more frequent in PCa group (p=0.0002)

Conclusions: Our data provide evidence for a role of PIA as a PCa precursor lesion as we observed a strong association between morphological transition PIA-HGPIN and PCa. As inflammation was observed in the vast majority of patient samples, our analysis did not detect an association with PCa. Likewise, a clear association between atrophy and PCa was not observed.